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In addition to its role in the central nervous system, MME has been reported to be expressed in the peripheral system, specifically in the inner and outer border of myelinating fibers, in the Schmidt\u2010Lantermann cleft and in the paranodes. Recently, mutations of this gene have been associated with Charcot\u2010Marie\u2010Tooth Type 2 (CMT2). Peripheral nerve morphometry in mice lacking MME previously showed minor abnormalities in aged animals in comparison to CMT2 patients. We found that MME expression was dysregulated after nerve injury in a Neuregulin\u20101 dependent fashion. We therefore explored the hypothesis that MME may have a role in remyelination. In the na\u00efve state in adulthood we did not find any impairment in myelination in MME KO mice. After nerve injury the morphological outcome in MME KO mice was indistinguishable from WT littermates in terms of axon regeneration and remyelination. We did not find any difference in functional motor recovery. There was a significant difference in sensory function, with MME KO mice starting to recover response to mechanical stimuli earlier than WT. The epidermal reinnnervation, however, was unchanged and this altered sensitivity may relate to its known function in cleaving the peptide substance\u2010P, known to sensitise nociceptors. In conclusion, although MME expression is dysregulated after nerve injury in a NRG1\u2010dependent manner this gene is dispensable for axon regeneration and remyelination after injury.<\/jats:p>","DOI":"10.1002\/glia.23680","type":"journal-article","created":{"date-parts":[[2019,7,24]],"date-time":"2019-07-24T11:18:17Z","timestamp":1563967097000},"page":"1990-2000","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Membrane metallo\u2010endopeptidase is dispensable for repair after nerve injury"],"prefix":"10.1002","volume":"67","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0078-1586","authenticated-orcid":false,"given":"Ilaria","family":"Cervellini","sequence":"first","affiliation":[{"name":"The Nuffield Department of Clinical Neurosciences University of Oxford, John Radcliffe Hospital  Oxford UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jorge","family":"Galino","sequence":"additional","affiliation":[{"name":"The Nuffield Department of Clinical Neurosciences University of Oxford, John Radcliffe Hospital  Oxford UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ning","family":"Zhu","sequence":"additional","affiliation":[{"name":"The Nuffield Department of Clinical Neurosciences University of Oxford, John Radcliffe Hospital  Oxford UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florence R.","family":"Fricker","sequence":"additional","affiliation":[{"name":"The Nuffield Department of Clinical Neurosciences University of Oxford, John Radcliffe Hospital  Oxford UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lu","family":"Bao","sequence":"additional","affiliation":[{"name":"Boston Children's Hospital Harvard Medical School  Boston Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David L. 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